【讨论】消化道出血病例，附英语文献学习
这个帖子发布于 12 年零 69 天前，其中的信息可能已发生改变或有所发展。
男，60岁
主诉： 间断上腹痛伴呕血、黑便9月余，加重4天。
现病史：患者自2012-5起无明显诱因间断出现清晨上腹部胀痛，VAS8分，无放射痛，伴乏力、大汗、胸闷，进食后略有缓解。每2月发作一次。发作前后有间断黑便及呕少量陈旧性血块。外院考虑为"消化性溃疡"（未行胃镜），予奥美拉唑口服治疗2~3天后腹痛消失，即自行停药，未规律诊治。患者2013-1-8清晨出现恶心、呕吐咖啡色胃内容物约50ml，排黑便1次，约300ml，伴胸闷、乏力、头晕、大汗。BP 129/74mmHg，血常规示HGB 113g/L。心电图示V4-V6 ST段下移0.1mv。予补液、扩冠等治疗，疗效不佳。1-9曾晕厥1次，无大小便失禁，补液后意识恢复。外院治疗期间血压最低为86/62mmHg，血常规示HGB进行性下降（113g/L→90g/L→81g/L）。1-10转至我院。入院BP 105/63mmHg，HR 103bpm。血常规：WBC 9.44×10^9/L，N% 79.6%，HGB 53g/L， PLT 199×10^9/L，HCT 15.8%。凝血：PT 12.8s，INR 1.14，Fbg 1.85g/L，APTT 25.4s，D-Dimer <0.15mg/L FEU。血生化：Alb 29g/L，Ca 1.80mmol/L，Urea 14.42mmol/L，Glu 8.1mmol/L，Cr(E) 82μmol/L，ALT 7U/L，AMY 144U/L，LIP 275U/L。予禁食水、胃管引流、补液、抑酸、止血、输血等治疗。患者于2013-1-10 夜间解黑色稀便约800ml，胃管引流出鲜红色血液约300ml，伴口干、乏力，BP 85/50mmHg，HR 112bpm。复查血常规 HGB 49g/L，考虑活动性出血，出血量大，于今晨行急诊胃镜，十二指肠球腔前下壁见梭形溃疡，表面血管显露，予钛夹两枚夹闭，1:10000肾上腺素盐水局部喷洒，观察无活动性出血。患者目前无呕血、黑便，无心慌、腹痛。现为进一步诊治收入病房。
患者否认NSAIDs类药物服用史。
既往史: 1995年及1997年曾有右侧输尿管结石，保守治疗后好转。饮酒30余年，每月1~2次，每次半斤白酒，已戒酒3年。
查体：T：37℃ P：94bpm R：17 f/min BP：121/68mmHg
Ht：172 cm Wt：87 kg BMI：29.41kg/m2 SpO2：100%（@RA，静息状态）
面色苍白，腹部及肛门直肠未查及异常，余未查及异常。
01-10全血细胞分析：WBC 12.35*10^9/L，NEUT% 66.8％，RBC 1.79*10^12/L，HGB 49g/L，HCT 15.0%，PLT 207*10^9/L。
凝血2：PT 12.8s，INR 1.14，Fbg 1.85g/L，APTT 25.4s，D-Dimer <0.15mg/L FEU。
肝肾功、胰功：Alb 29g/L，Ca 1.80mmol/L，Urea 14.42mmol/L，Glu 8.1mmol/L，Cr(E) 82μmol/L，ALT 7U/L，AMY 144U/L，LIP 275U/L。
2013-01-11
全血细胞分析：WBC 15.47*10^9/L，NEUT% 91.3％，LY% 5.9％，RBC 1.53*10^12/L，HGB 45g/L，HCT 13.4%，PLT 145*10^9/L。
肝肾功、胰功：K 4.7mmol/L，Na 136mmol/L，Ca 1.79mmol/L，Glu 17.9mmol/L，Urea 14.25mmol/L，Cr(E) 101μmol/L，AMY 192U/L，LIP 468U/L。
心脏3项：CK 70U/L，CKMB-mass 0.5μg/L，cTnI 0.050μg/L，
血脂4项：TC 2.13mmol/L，TG 2.20mmol/L，HDL-C 0.42mmol/L，LDL-C 1.10mmol/L。
胃镜：十二指肠球腔、球后及降部可见新鲜血迹，球部为著。冲洗后于球腔前下壁见梭形溃疡，表面血管显露，缓慢渗血。予钛夹夹闭及1:10000肾上腺素盐水20ml局部喷洒后，观察无活动性出血。球后另见一圆形深溃疡，表覆白苔，无活动性出血。
1. 上、下消化道出血的鉴别;2. 上消化道出血的常见病因及鉴别;3. 急性消化道出血的病情;评估;4. 急性消化道出血的常用治疗手段及处理流程;5. 再出血的常见表现;6. 消化性溃疡的常见并发症;7. （可选）常见的生长抑素类药物及使用方法;8. （可选）针对该患者，你会选择怎样的营养支持方案？
Background/Aim:
The prevalence of acute upper gastrointestinal bleeding (AUGIB) has undergone a change after implementation of eradication therapy for Helicobacter pylori in peptic ulcers effective prevention of esophageal variceal bleeding and eventually, progressive use of low dose aspirin and other nonsteroidal antiinflammatory drugs (NSAIDs). To evaluate this subject, we performed a prospective study in two main University Hospitals of Shiraz (the largest city of southern Iran).
Materials and Methods:
All adults who were admitted in emergency room with impression of AUGIB and existing patients who developed AUGIB were included in the study. Gastroscopy was done with a follow-up for the next 15 days.
Results:
572 patients (mean age: 54.9 years) entered in the study. The most common presenting symptom was hematemesis or coffee-ground vomits (68%). 75% of patients gave history of consumption of low dose aspirin or other NSAIDs regularly. Gastric and/or duodenal ulcers were the most common causes (252/572, 44%) of AUGIB (Gastric ulcer: 173/572, 30% and duodenal ulcer: 93/572, 16%, respectively). Esophageal varices were the third common cause (64/572, 11%). 36 (6%) of the patients died. Mean age of these patients was higher than the patients who were alive (64.8 vs. 54.2 years, P = 0.001). Other than age, orthostatic hypotension on arrival (267/536 vs. 24/36, P = 0.018) and consumption of steroids (43/536 vs. 10/36, P = 0.001) were significant factors for increasing mortality.
Conclusions:
The most common cause of AUGIB, secondary only to NSAIDs consumption, is gastric ulcer. Mortality of older patients, patients who consumed NSAIDs and steroids concomitantly, and patients with hemodynamic instability on arrival were higher.
Keywords:Acute upper gastrointestinal bleeding, gastric ulcer, nonsteroidal antiinflammatory drugs
Acute upper gastrointestinal bleeding (AUGIB) remains a common emergency and potentially fatal situation that requires hospitalization. The incidence of AUGIB varies between 50-150 hospital admissions per 100,000 population in a year[1–5] (approximately 1% of all emergency room admissions).
Approximately 45–60% of admissions for AUGIB worldwide are due to peptic ulcers followed by esophagitis and esophageal varices.[2,6] Although, H. pylori infection has been one of the most common causes of peptic ulcer disease, and eventually AUGIB, in the developing countries in the last few years, it seems that due to better sanitation, better diagnostic and therapeutic approaches, rate of AUGIB secondary to H. pylori infection has been decreased.[4,7,8] On the other hand, excessive usage of low dose aspirin for primary or secondary prevention of atherosclerotic heart and brain diseases, increasing life expectancy and so increasing rate of degenerative joint disease and osteoarthropathies and excessive ingestion of other nonsteroidal antiinflammatory drugs (NSAIDS), may change the incidence, age of presentation, site of bleeding and outcome of patients with nonvariceal AUGIB in the last decade.[7,8]
It seems that better sanitation, vaccination against Hepatitis B virus, prophylactic using of propranolol, esophageal band ligation and liver transplantation has changed the incidence of esophageal variceal bleeding.[9]
Common use of high dose proton pump inhibitors, better availability of diagnostic and therapeutic endoscopy and increasing cost of hospitalization may change the economic burden of AUGIB.[10]
Despite the fact that epidemiologic data are important to get insight into the actual situation,[11] there is no epidemiologic survey regarding AUGIB in our area.
The aim of this study was to survey the etiology and clinical outcome of AUGIB in referred and already hospitalized patients of two hospitals in Shiraz.
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MATERIALS AND METHODS
We prospectively evaluated clinical characteristics, cause of bleeding and clinical outcome, of 383 referred (de novo) and 189 already admitted (inpatients) referred to the Faghihi Hospital and Namazi Hospital.
Patients
De novo patients: All adult patients (≥16 years old) who were admitted in emergency room with impression of AUGIB by internal medicine residents for more than 8 hours, were included in the study. All patients were admitted with a history of malaena or hematemesis on the day of admission
Ongoing hematemesis/melena
This was defined as a history of melena/hematemesis several days before admission and decrease in the hemoglobin level (>1gm/dl), shock (blood pressure <90/60 mmHg in supine position), pallor, orthostatic hypotension (>20 mmHg decrease in systolic blood pressure or >10mmHg in diastolic blood pressure from supine to standing position), or anemia (hemoglobin < 12 gm/dl and <14 gm/dl in female and male respectively), insertion of naso-gastric tube and suction of fresh blood or coffee-ground materials without clearance of gastric washing by 250 cc of isotonic solution and exclusion of other causes of false AUGIB, such as bleeding from upper respiratory tract, nose bleeding, bleeding from paranasal sinuses, etc.
In-hospital patients: AUGIB in hospital adult (≥16 years old) patients were confirmed with nonclearance of gastric washing by 250 cc of isotonic solution, positive stool occult blood test and no evidence of active bleeding from upper respiratory tract.
After enrolment in the study, a questionnaire including demographic data, important points in the history, physical exam and laboratory tests such as history of acid peptic disease, presence of cirrhosis, cause of cirrhosis, NSAID use, regular ingestion of low dose aspirin, previous history of AUGIB and cause of it, co-morbidities, ongoing vital signs, pallor, organomegaly, ascites, ongoing and 6 hour after admission hemoglobin (Hgb), activated prothrombin time (PT), platelet (Plt), partial thromboplastin time (PTT) etc was filled by research assistants. Upper GI endoscopy was performed by our on-call fellow or attending physician within 24 hours of admission. There was a daily follow-up of patients after admission and up to 15 days after being discharged from hospital. End points including mortality, re-bleeding in hospital and within 15 days after discharge, blood transfusion and surgery were registered.
Statistical analysis
Statistical package for social sciences (SPSS, version 15.0; Chicago, IL, USA) and Epi Info 2000 programs were used for data analysis. Student T-test was used for quantitative and Chi-square and Fisher exact tests were used for qualitative variables.
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RESULTS
Five hundred and seventy two patients (including 383 de novo and 189 in-hospital) entered the study, of which 377 (66%) were male. The mean age of our patients was 54.9 years (±SD: 18.7). Other demographic data are shown in Table 1.
Table 1
Comparison and common complaints of patients with upper gastrointestinal bleeding
The most common symptom on presentation was hematemesis or coffee-ground vomits (68%) followed by melena (38%) in our patients. Sixteen percent of our patients gave history of acid peptic disease and 75% of them consumed low dose aspirin or other NSAIDs (except for celecoxib) regularly. Other basic histories are shown in Table 1. On admission, 42% of our patients had orthostatic hypotension, with a mean hemoglobin level of 10.9 gm/ dl [Table 2].
Table 2
Clinical features on admission and primary laboratory results of patients with de novo upper gastrointestinal bleeding
Gastric ulcer was the most common finding in upper endoscopy. One hundred and seventy three patients had gastric ulcer (124/383, 32% and 49/189, 26% of de novo and in-hospital patients, respectively). The most common site was lesser curvature (57/173, 33%) and only 87/173 (50%) of these ulcers fulfilled criteria of low risk ulcer for rebleeding. Duodenal ulcer was present in 93 patient (62/383, 16%, and 31/189, 16% of de novo and in-hospital patients, respectively). 55/93 (59%) of these ulcers fulfilled criteria of low risk ulcer for re-bleeding. Esophageal varices were found in 64 patients (47/383, 12% and 17/189, 9% of de novo and in-hospital patients respectively). Eight of these patients had gastric ulcer (four Clean-based, one with oozing of blood from ulcer bed, and three with visible vessel) and five of them had clean based duodenal ulcer. Less than 10% of our patients had gastritis or Mallory-Weiss’ tears as the causes of AUGIB and 99/572 (17%) of our patients had normal upper endoscopy [Table 3].
Table 3
Result of primary endoscopy in de novo and in-hospital patients with upper gastrointestinal bleeding
Injection therapy and/or argon plasma coagulation was done for 54 patients with high risk ulcers and 12 (22%) of them had high risk ulcers in second look endoscopy. Blood transfusion was required in 197 patients and finally, mortality rate of our patients was 6% for de novo and 7% for in-hospital patients respectively [Table 4].
Table 4
End points in de novo and in-hospital patients with upper gastrointestinal bleeding
The mortality rate was higher in older patients, patients with orthostatic hypotension on arrival and patients who consumed steroids [Table 5].
Table 5
Comparison between alive and deceased patients with upper gastrointestinal bleeding
Analysis showed that mortality was directly related to increase in age [Table 6].
Table 6
The mortality rate and age of patients with upper gastrointestinal bleeding
Comparison between ≤60 and >60 years old patients showed that older patients had more serious presentations (hematemesis or coffee-ground vomits, orthostatic hypotension or shock on arrival). They consumed aspirin, alcohol, steroids, warfarin, smoked water-pipe and cigarettes more than younger patients and eventually, acid peptic disease as the cause of AUGIB was more frequent in older patients [Table 7]. Thirty four patients who consumed steroids in this age group, also consumed aspirin or other NSAIDs and seven of these patients died. Acid peptic disease as the cause/s of AUGIB was more frequently found in older patients [Table 7].
Table 7
Comparison between younger (≤60 years) and older (>60 years) patients with upper gastrointestinal bleeding
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DISCUSSION
Because of shortcomings in records, this study was done prospectively with predefined strategy and goals in the two largest referral centers in southern Iran i.e., Faghihi and Namazi Hospitals.
Only patients who were admitted in hospital for a minimum of 8 hours were considered for the study and followed up to the end point, so automatically patients with minor bleeding were excluded. As a result, in our study the most common presentation of AUGIB was hematemesis or vomiting of coffee-ground material in both de novo and in-hospital patients [Table 1]; orthostatic hypotension was seen in 291 (51%) of patients, the most common cause of AUGIB was acid peptic disease and not gastritis (such as study of Boonpongmanee S. et al[5]), and only 63/173 (36%) of gastric ulcers and 46/93 (49%) of duodenal ulcers were clean-based.
As a developing country, statistical analysis of demographic data in this survey showed that there is no difference between our results in sex (66% male) and mean age (54.9 year old) in comparison with the same studies in developed countries.[2,4]
Due to progressive and drastic changes in medical and health care systems, the age and life expectancy of general population has been increasing in Iran, and in this way some of the common geriatric problems such as coronary artery disease, degenerative joint disease and osteoarthropathies and eventually excessive consumption of all kinds of NSAIDs and low dose aspirin as main standard therapies has increased. It seems that this expansive usage of these drugs led to increasing rate of GU as a cause of AUGIB and this may be comparable with results of Enestvedt et al.[1] On the other hand, according to the above facts and considering the effective newer and widespread management of H. pylori as a major cause of peptic ulcer and gastric cancer, introducing gastric ulcer as a new leading cause of AUGIB is confirmed by our study (GU 30%, DU 16%).[10,12] Meanwhile, the decreasing rate of variceal bleeding (11%) may be explained by the extensive usage of effective drugs for chronic hepatitis/cirrhosis caused by hepatitis B and C viruses and autoimmune hepatitis, in addition to a vast usage of propanolol and rubber band ligation as primary prevention methods for variceal bleeding.
Comparing similar studies,[13] the reduction in hospital stay, from a standard 5.5 days to 2.2 days, can be explained by better management of AUGIB.
Mortality rate of AUGIB in our centers was comparable to centers in developed countries.[11] We compared some of the data between alive and deceased patients.
The first finding was mean age (54 vs. 65 years, P = 0.001). Mortality rate was significantly different for. 60 years (4%) versus >60 years (10%, P = 0.003). Further analysis showed that this finding may be secondary to more blood loss before referral [Table 7] and frequent consumption of aspirin or other anticoagulants.[3,14] Further, this is also secondary to concomitant diseases such as ischemic heart disease and cerebro-vascular accident, which have a higher frequency in older patients. Acid peptic disease as the major cause of AUGIB was more frequent in older patients (40% in younger vs 49% in older patients respectively, P = 0.028). The second finding in deceased patients was past history of steroids usage which also was statistically different (8% in alive Vs 28% in deceased patients respectively, P = 0.001). External steroids, by themselves, are not harmful for stomach or duodenum but concomitant use of steroids and NSAIDs usually increase the risk of gastric and duodenal ulceration and AUGIB.[15] Our study showed (just like Shorr et al findings)[16] that concomitant use of steroids and NSAIDs may also increase the mortality secondary to AUGIB in this subset of patients. 45 out of 53 (85%) steroids users concomitantly used NSAIDs, while 7 out of 10 died due to AUGIB.
Acute (15-day) mortality rate in patients with esophageal variceal bleeding (5/64, 8%) was comparable with other nonvariceal causes such as acid peptic disease (13/252, 5%) and this may be secondary to better management of these patients and/or use of newer therapeutic modalities to stop the bleeding in this group. This result agrees with findings of Chalasani N et al.[9]
In conclusion, it appears that the most common cause of AUGIB is acid peptic disease, which increases with the age of the patient, and frequent consumption of NSAIDs, and gastric ulcer as the main source of bleeding may be NSAIDs induced. It is therefore suggested to take a thorough history pertaining to acid peptic disease, before the start of aspirin, and decrease the threshold of performing upper gastrointestinal endoscopy and possibly prescription of proton pump inhibitors especially in high risk groups (older age, concurrent anticoagulant, or steroid users, etc). Furthermore eradication of H. pylori prior to starting aspirin or other NSAIDs may decrease the rate of AUGIB secondary to acid peptic disease.[11] Finally, in this regard, consideration of international recommendations on starting aspirin or other NSAIDs will be helpful.
主诉： 间断上腹痛伴呕血、黑便9月余，加重4天。
现病史：患者自2012-5起无明显诱因间断出现清晨上腹部胀痛，VAS8分，无放射痛，伴乏力、大汗、胸闷，进食后略有缓解。每2月发作一次。发作前后有间断黑便及呕少量陈旧性血块。外院考虑为"消化性溃疡"（未行胃镜），予奥美拉唑口服治疗2~3天后腹痛消失，即自行停药，未规律诊治。患者2013-1-8清晨出现恶心、呕吐咖啡色胃内容物约50ml，排黑便1次，约300ml，伴胸闷、乏力、头晕、大汗。BP 129/74mmHg，血常规示HGB 113g/L。心电图示V4-V6 ST段下移0.1mv。予补液、扩冠等治疗，疗效不佳。1-9曾晕厥1次，无大小便失禁，补液后意识恢复。外院治疗期间血压最低为86/62mmHg，血常规示HGB进行性下降（113g/L→90g/L→81g/L）。1-10转至我院。入院BP 105/63mmHg，HR 103bpm。血常规：WBC 9.44×10^9/L，N% 79.6%，HGB 53g/L， PLT 199×10^9/L，HCT 15.8%。凝血：PT 12.8s，INR 1.14，Fbg 1.85g/L，APTT 25.4s，D-Dimer <0.15mg/L FEU。血生化：Alb 29g/L，Ca 1.80mmol/L，Urea 14.42mmol/L，Glu 8.1mmol/L，Cr(E) 82μmol/L，ALT 7U/L，AMY 144U/L，LIP 275U/L。予禁食水、胃管引流、补液、抑酸、止血、输血等治疗。患者于2013-1-10 夜间解黑色稀便约800ml，胃管引流出鲜红色血液约300ml，伴口干、乏力，BP 85/50mmHg，HR 112bpm。复查血常规 HGB 49g/L，考虑活动性出血，出血量大，于今晨行急诊胃镜，十二指肠球腔前下壁见梭形溃疡，表面血管显露，予钛夹两枚夹闭，1:10000肾上腺素盐水局部喷洒，观察无活动性出血。患者目前无呕血、黑便，无心慌、腹痛。现为进一步诊治收入病房。
患者否认NSAIDs类药物服用史。
既往史: 1995年及1997年曾有右侧输尿管结石，保守治疗后好转。饮酒30余年，每月1~2次，每次半斤白酒，已戒酒3年。
查体：T：37℃ P：94bpm R：17 f/min BP：121/68mmHg
Ht：172 cm Wt：87 kg BMI：29.41kg/m2 SpO2：100%（@RA，静息状态）
面色苍白，腹部及肛门直肠未查及异常，余未查及异常。
01-10全血细胞分析：WBC 12.35*10^9/L，NEUT% 66.8％，RBC 1.79*10^12/L，HGB 49g/L，HCT 15.0%，PLT 207*10^9/L。
凝血2：PT 12.8s，INR 1.14，Fbg 1.85g/L，APTT 25.4s，D-Dimer <0.15mg/L FEU。
肝肾功、胰功：Alb 29g/L，Ca 1.80mmol/L，Urea 14.42mmol/L，Glu 8.1mmol/L，Cr(E) 82μmol/L，ALT 7U/L，AMY 144U/L，LIP 275U/L。
2013-01-11
全血细胞分析：WBC 15.47*10^9/L，NEUT% 91.3％，LY% 5.9％，RBC 1.53*10^12/L，HGB 45g/L，HCT 13.4%，PLT 145*10^9/L。
肝肾功、胰功：K 4.7mmol/L，Na 136mmol/L，Ca 1.79mmol/L，Glu 17.9mmol/L，Urea 14.25mmol/L，Cr(E) 101μmol/L，AMY 192U/L，LIP 468U/L。
心脏3项：CK 70U/L，CKMB-mass 0.5μg/L，cTnI 0.050μg/L，
血脂4项：TC 2.13mmol/L，TG 2.20mmol/L，HDL-C 0.42mmol/L，LDL-C 1.10mmol/L。
胃镜：十二指肠球腔、球后及降部可见新鲜血迹，球部为著。冲洗后于球腔前下壁见梭形溃疡，表面血管显露，缓慢渗血。予钛夹夹闭及1:10000肾上腺素盐水20ml局部喷洒后，观察无活动性出血。球后另见一圆形深溃疡，表覆白苔，无活动性出血。
1. 上、下消化道出血的鉴别;2. 上消化道出血的常见病因及鉴别;3. 急性消化道出血的病情;评估;4. 急性消化道出血的常用治疗手段及处理流程;5. 再出血的常见表现;6. 消化性溃疡的常见并发症;7. （可选）常见的生长抑素类药物及使用方法;8. （可选）针对该患者，你会选择怎样的营养支持方案？
Background/Aim:
The prevalence of acute upper gastrointestinal bleeding (AUGIB) has undergone a change after implementation of eradication therapy for Helicobacter pylori in peptic ulcers effective prevention of esophageal variceal bleeding and eventually, progressive use of low dose aspirin and other nonsteroidal antiinflammatory drugs (NSAIDs). To evaluate this subject, we performed a prospective study in two main University Hospitals of Shiraz (the largest city of southern Iran).
Materials and Methods:
All adults who were admitted in emergency room with impression of AUGIB and existing patients who developed AUGIB were included in the study. Gastroscopy was done with a follow-up for the next 15 days.
Results:
572 patients (mean age: 54.9 years) entered in the study. The most common presenting symptom was hematemesis or coffee-ground vomits (68%). 75% of patients gave history of consumption of low dose aspirin or other NSAIDs regularly. Gastric and/or duodenal ulcers were the most common causes (252/572, 44%) of AUGIB (Gastric ulcer: 173/572, 30% and duodenal ulcer: 93/572, 16%, respectively). Esophageal varices were the third common cause (64/572, 11%). 36 (6%) of the patients died. Mean age of these patients was higher than the patients who were alive (64.8 vs. 54.2 years, P = 0.001). Other than age, orthostatic hypotension on arrival (267/536 vs. 24/36, P = 0.018) and consumption of steroids (43/536 vs. 10/36, P = 0.001) were significant factors for increasing mortality.
Conclusions:
The most common cause of AUGIB, secondary only to NSAIDs consumption, is gastric ulcer. Mortality of older patients, patients who consumed NSAIDs and steroids concomitantly, and patients with hemodynamic instability on arrival were higher.
Keywords:Acute upper gastrointestinal bleeding, gastric ulcer, nonsteroidal antiinflammatory drugs
Acute upper gastrointestinal bleeding (AUGIB) remains a common emergency and potentially fatal situation that requires hospitalization. The incidence of AUGIB varies between 50-150 hospital admissions per 100,000 population in a year[1–5] (approximately 1% of all emergency room admissions).
Approximately 45–60% of admissions for AUGIB worldwide are due to peptic ulcers followed by esophagitis and esophageal varices.[2,6] Although, H. pylori infection has been one of the most common causes of peptic ulcer disease, and eventually AUGIB, in the developing countries in the last few years, it seems that due to better sanitation, better diagnostic and therapeutic approaches, rate of AUGIB secondary to H. pylori infection has been decreased.[4,7,8] On the other hand, excessive usage of low dose aspirin for primary or secondary prevention of atherosclerotic heart and brain diseases, increasing life expectancy and so increasing rate of degenerative joint disease and osteoarthropathies and excessive ingestion of other nonsteroidal antiinflammatory drugs (NSAIDS), may change the incidence, age of presentation, site of bleeding and outcome of patients with nonvariceal AUGIB in the last decade.[7,8]
It seems that better sanitation, vaccination against Hepatitis B virus, prophylactic using of propranolol, esophageal band ligation and liver transplantation has changed the incidence of esophageal variceal bleeding.[9]
Common use of high dose proton pump inhibitors, better availability of diagnostic and therapeutic endoscopy and increasing cost of hospitalization may change the economic burden of AUGIB.[10]
Despite the fact that epidemiologic data are important to get insight into the actual situation,[11] there is no epidemiologic survey regarding AUGIB in our area.
The aim of this study was to survey the etiology and clinical outcome of AUGIB in referred and already hospitalized patients of two hospitals in Shiraz.
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MATERIALS AND METHODS
We prospectively evaluated clinical characteristics, cause of bleeding and clinical outcome, of 383 referred (de novo) and 189 already admitted (inpatients) referred to the Faghihi Hospital and Namazi Hospital.
Patients
De novo patients: All adult patients (≥16 years old) who were admitted in emergency room with impression of AUGIB by internal medicine residents for more than 8 hours, were included in the study. All patients were admitted with a history of malaena or hematemesis on the day of admission
Ongoing hematemesis/melena
This was defined as a history of melena/hematemesis several days before admission and decrease in the hemoglobin level (>1gm/dl), shock (blood pressure <90/60 mmHg in supine position), pallor, orthostatic hypotension (>20 mmHg decrease in systolic blood pressure or >10mmHg in diastolic blood pressure from supine to standing position), or anemia (hemoglobin < 12 gm/dl and <14 gm/dl in female and male respectively), insertion of naso-gastric tube and suction of fresh blood or coffee-ground materials without clearance of gastric washing by 250 cc of isotonic solution and exclusion of other causes of false AUGIB, such as bleeding from upper respiratory tract, nose bleeding, bleeding from paranasal sinuses, etc.
In-hospital patients: AUGIB in hospital adult (≥16 years old) patients were confirmed with nonclearance of gastric washing by 250 cc of isotonic solution, positive stool occult blood test and no evidence of active bleeding from upper respiratory tract.
After enrolment in the study, a questionnaire including demographic data, important points in the history, physical exam and laboratory tests such as history of acid peptic disease, presence of cirrhosis, cause of cirrhosis, NSAID use, regular ingestion of low dose aspirin, previous history of AUGIB and cause of it, co-morbidities, ongoing vital signs, pallor, organomegaly, ascites, ongoing and 6 hour after admission hemoglobin (Hgb), activated prothrombin time (PT), platelet (Plt), partial thromboplastin time (PTT) etc was filled by research assistants. Upper GI endoscopy was performed by our on-call fellow or attending physician within 24 hours of admission. There was a daily follow-up of patients after admission and up to 15 days after being discharged from hospital. End points including mortality, re-bleeding in hospital and within 15 days after discharge, blood transfusion and surgery were registered.
Statistical analysis
Statistical package for social sciences (SPSS, version 15.0; Chicago, IL, USA) and Epi Info 2000 programs were used for data analysis. Student T-test was used for quantitative and Chi-square and Fisher exact tests were used for qualitative variables.
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RESULTS
Five hundred and seventy two patients (including 383 de novo and 189 in-hospital) entered the study, of which 377 (66%) were male. The mean age of our patients was 54.9 years (±SD: 18.7). Other demographic data are shown in Table 1.
Table 1
Comparison and common complaints of patients with upper gastrointestinal bleeding
The most common symptom on presentation was hematemesis or coffee-ground vomits (68%) followed by melena (38%) in our patients. Sixteen percent of our patients gave history of acid peptic disease and 75% of them consumed low dose aspirin or other NSAIDs (except for celecoxib) regularly. Other basic histories are shown in Table 1. On admission, 42% of our patients had orthostatic hypotension, with a mean hemoglobin level of 10.9 gm/ dl [Table 2].
Table 2
Clinical features on admission and primary laboratory results of patients with de novo upper gastrointestinal bleeding
Gastric ulcer was the most common finding in upper endoscopy. One hundred and seventy three patients had gastric ulcer (124/383, 32% and 49/189, 26% of de novo and in-hospital patients, respectively). The most common site was lesser curvature (57/173, 33%) and only 87/173 (50%) of these ulcers fulfilled criteria of low risk ulcer for rebleeding. Duodenal ulcer was present in 93 patient (62/383, 16%, and 31/189, 16% of de novo and in-hospital patients, respectively). 55/93 (59%) of these ulcers fulfilled criteria of low risk ulcer for re-bleeding. Esophageal varices were found in 64 patients (47/383, 12% and 17/189, 9% of de novo and in-hospital patients respectively). Eight of these patients had gastric ulcer (four Clean-based, one with oozing of blood from ulcer bed, and three with visible vessel) and five of them had clean based duodenal ulcer. Less than 10% of our patients had gastritis or Mallory-Weiss’ tears as the causes of AUGIB and 99/572 (17%) of our patients had normal upper endoscopy [Table 3].
Table 3
Result of primary endoscopy in de novo and in-hospital patients with upper gastrointestinal bleeding
Injection therapy and/or argon plasma coagulation was done for 54 patients with high risk ulcers and 12 (22%) of them had high risk ulcers in second look endoscopy. Blood transfusion was required in 197 patients and finally, mortality rate of our patients was 6% for de novo and 7% for in-hospital patients respectively [Table 4].
Table 4
End points in de novo and in-hospital patients with upper gastrointestinal bleeding
The mortality rate was higher in older patients, patients with orthostatic hypotension on arrival and patients who consumed steroids [Table 5].
Table 5
Comparison between alive and deceased patients with upper gastrointestinal bleeding
Analysis showed that mortality was directly related to increase in age [Table 6].
Table 6
The mortality rate and age of patients with upper gastrointestinal bleeding
Comparison between ≤60 and >60 years old patients showed that older patients had more serious presentations (hematemesis or coffee-ground vomits, orthostatic hypotension or shock on arrival). They consumed aspirin, alcohol, steroids, warfarin, smoked water-pipe and cigarettes more than younger patients and eventually, acid peptic disease as the cause of AUGIB was more frequent in older patients [Table 7]. Thirty four patients who consumed steroids in this age group, also consumed aspirin or other NSAIDs and seven of these patients died. Acid peptic disease as the cause/s of AUGIB was more frequently found in older patients [Table 7].
Table 7
Comparison between younger (≤60 years) and older (>60 years) patients with upper gastrointestinal bleeding
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DISCUSSION
Because of shortcomings in records, this study was done prospectively with predefined strategy and goals in the two largest referral centers in southern Iran i.e., Faghihi and Namazi Hospitals.
Only patients who were admitted in hospital for a minimum of 8 hours were considered for the study and followed up to the end point, so automatically patients with minor bleeding were excluded. As a result, in our study the most common presentation of AUGIB was hematemesis or vomiting of coffee-ground material in both de novo and in-hospital patients [Table 1]; orthostatic hypotension was seen in 291 (51%) of patients, the most common cause of AUGIB was acid peptic disease and not gastritis (such as study of Boonpongmanee S. et al[5]), and only 63/173 (36%) of gastric ulcers and 46/93 (49%) of duodenal ulcers were clean-based.
As a developing country, statistical analysis of demographic data in this survey showed that there is no difference between our results in sex (66% male) and mean age (54.9 year old) in comparison with the same studies in developed countries.[2,4]
Due to progressive and drastic changes in medical and health care systems, the age and life expectancy of general population has been increasing in Iran, and in this way some of the common geriatric problems such as coronary artery disease, degenerative joint disease and osteoarthropathies and eventually excessive consumption of all kinds of NSAIDs and low dose aspirin as main standard therapies has increased. It seems that this expansive usage of these drugs led to increasing rate of GU as a cause of AUGIB and this may be comparable with results of Enestvedt et al.[1] On the other hand, according to the above facts and considering the effective newer and widespread management of H. pylori as a major cause of peptic ulcer and gastric cancer, introducing gastric ulcer as a new leading cause of AUGIB is confirmed by our study (GU 30%, DU 16%).[10,12] Meanwhile, the decreasing rate of variceal bleeding (11%) may be explained by the extensive usage of effective drugs for chronic hepatitis/cirrhosis caused by hepatitis B and C viruses and autoimmune hepatitis, in addition to a vast usage of propanolol and rubber band ligation as primary prevention methods for variceal bleeding.
Comparing similar studies,[13] the reduction in hospital stay, from a standard 5.5 days to 2.2 days, can be explained by better management of AUGIB.
Mortality rate of AUGIB in our centers was comparable to centers in developed countries.[11] We compared some of the data between alive and deceased patients.
The first finding was mean age (54 vs. 65 years, P = 0.001). Mortality rate was significantly different for. 60 years (4%) versus >60 years (10%, P = 0.003). Further analysis showed that this finding may be secondary to more blood loss before referral [Table 7] and frequent consumption of aspirin or other anticoagulants.[3,14] Further, this is also secondary to concomitant diseases such as ischemic heart disease and cerebro-vascular accident, which have a higher frequency in older patients. Acid peptic disease as the major cause of AUGIB was more frequent in older patients (40% in younger vs 49% in older patients respectively, P = 0.028). The second finding in deceased patients was past history of steroids usage which also was statistically different (8% in alive Vs 28% in deceased patients respectively, P = 0.001). External steroids, by themselves, are not harmful for stomach or duodenum but concomitant use of steroids and NSAIDs usually increase the risk of gastric and duodenal ulceration and AUGIB.[15] Our study showed (just like Shorr et al findings)[16] that concomitant use of steroids and NSAIDs may also increase the mortality secondary to AUGIB in this subset of patients. 45 out of 53 (85%) steroids users concomitantly used NSAIDs, while 7 out of 10 died due to AUGIB.
Acute (15-day) mortality rate in patients with esophageal variceal bleeding (5/64, 8%) was comparable with other nonvariceal causes such as acid peptic disease (13/252, 5%) and this may be secondary to better management of these patients and/or use of newer therapeutic modalities to stop the bleeding in this group. This result agrees with findings of Chalasani N et al.[9]
In conclusion, it appears that the most common cause of AUGIB is acid peptic disease, which increases with the age of the patient, and frequent consumption of NSAIDs, and gastric ulcer as the main source of bleeding may be NSAIDs induced. It is therefore suggested to take a thorough history pertaining to acid peptic disease, before the start of aspirin, and decrease the threshold of performing upper gastrointestinal endoscopy and possibly prescription of proton pump inhibitors especially in high risk groups (older age, concurrent anticoagulant, or steroid users, etc). Furthermore eradication of H. pylori prior to starting aspirin or other NSAIDs may decrease the rate of AUGIB secondary to acid peptic disease.[11] Finally, in this regard, consideration of international recommendations on starting aspirin or other NSAIDs will be helpful.
